A new study suggests that Memantine, a drug currently approved for treatment of the late stages of Alzheimer's disease, might also be effective in early stages.

In animal based experiments, rats were taught to find their way through a water maze and then given agents to induce brain inflammation. Consistent with theories suggesting that inflammation impairs cognitive function, the rats essentially "forgot" how to navigate the maze. However, once given Memantine, the rats' performance normalized and they were once again able to complete the maze.

Obviously, this is early-stage work but the hypothesis has theoretical validity and the earliest empirical data are encouraging.

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Based on the various interpretations I read in the press, there seems to be some confusion about the term dementia. The DSM-IV (Diagnostic and Statistical Manual for Mental Disorders, American Psychiatric Association) provides the most commonly used criteria and defines dementia in this way:

Dementia is a clinical state characterized by loss of function in multiple cognitive domains. Diagnostic features include : memory impairment and at least one of the following: aphasia, apraxia, agnosia, disturbances in executive functioning. In addition, the cognitive impairments must be severe enough to cause impairment in social and occupational functioning.

So, in even simpler terms, being demented means that one's mental faculties are impaired to a degree that interferes with their social and occupational function. For the purpose of most discussions, it really is as simple as that.

The confusion begins when people talk about "being diagnosed with dementia" or "treating dementia". In a world of clarity, those same people would speak instead about "being diagnosed with Parkinson's Disease or with Alzheimer's Disease" which may have led to a clinical state of dementia. No one would "treat dementia", they would treat the underlying medical condition causing the impairment that we describe as dementia. It is a simple concept but I hear it confused (or read about it being confused) on a daily basis.

We don't need to detect dementia, we need to detect medical conditions that lead to dementia. We cannot treat dementia, we must treat medical conditions that cause dementia. The word dementia merely describes the extent of some person's cognitive impairment.

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We are virtually swimming (if not drowning) in the evidence that managing your vascular health may be the best approach to maintaining a healthy brain. In the past few days, I have blogged about several studies on this topic and many more have been published in the scientific literature.

To emphasize this important theme, here is a quick review of the very recent evidence:

This study out of UCLA and published in Human Brain Mapping showed a strong link between obesity and less brain tissue.

According to Helpguide.org and many other sources, vascular disease follows Alzheimer's disease as the second leading cause of dementia.

As described in this post about strokes, one may be quite different from another but all impair cognition and vascular risk factors almost always play a role.

Diet and exercise matter for both vascular and cognitive health. This has been repeatedly verified through careful research and will continue to be a popular theme in the news.

In surprising news, Kaiser Permanente published research showing that even borderline high cholesterol significantly raised the risk of dementia.

The facts are abundant. Please take care of your vascular health and keep that brain functioning at a high level.

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We have seen much press about the promise of advanced tracers and binding agents that improve the ability of imaging technologies to identify signs of early stage Alzheimer's disease. Due to the popularity of the amyloid hypothesis, suggesting that beta amyloid plaques are a key culprit in Alzheimer's pathology, research on agents that bind to amyloid have been especially present in the recent literature.

A study now published in Neurology suggests that functional MRI might also be useful in detecting early signs of Alzheimer's disease. In a study conducted at Cleveland Clinic’s Lou Ruvo Center for Brain Health, a group of 69 cognitively healthy adults, some of whom were genetically at risk to develop Alzheimer’s disease, were evaluated. Functional MRI was used to measure the participant's brain activity during a series of recognition tasks and the results of the at-risk group were compared to the results of the others.

The results showed an increased activation of certain parts of the brain in at-risk individuals which may reflect a compensatory brain response by those in the earliest stages of Alzheimer’s disease. If so, fMRI could prove to be a key technology for earlier identification of and intervention against emerging Alzheimer's disease.

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Contributed by: Michael Rafii, M.D., Ph.D - Director of the Memory Disorders Clinic at the University of California, San Diego. _______________________________

Nano particles are named for their small size (a nanometer is a billionth of a meter), and nano particles are smaller than anything humans have ever put into commercial products before, including sunscreen.

The smaller an object is, the larger its surface is in relation to its volume. Thus nano particles have an enormous surface to volume ratio, which renders them biologically active. This increased biologic activity can be either positive and desirable (e.g., antioxidant activity, carrier capacity for therapeutics, penetration of cellular barriers for drug delivery) or negative and undesirable (e.g., toxicity, induction of oxidative stress or of cellular dysfunction), or a mix of both.

Now public interest organizations are asking the FDA to 'Declare all currently available sunscreen drug products containing engineered nanoparticles of zinc oxide and titanium dioxide as an imminent hazard to public health.'

The nanoworld is quite a different place -- a world where particles can pass directly from the environment into your bloodstream, tissues, cells and organelles. There are three typical ways in which nanomaterials get into our bodies -- we breathe them, ingest them or absorb them through our skin. And despite the evidence that nanomaterials cause lung, liver and brain damage in animals, our Food and Drug Administration (FDA) is treating nanomaterials like their standard or bulk sized counterparts of yesteryear.

Once in the blood stream, nanomaterials can affect all of the organs and tissues of the body including the bone marrow, heart, lungs, brain, liver, spleen and kidneys. But little is known about what dose may cause harmful effects or how long different nanomaterials remain in various tissues.

Certainly more research is needed to answer the question of what effect nanoparticle may have on the human body, including the brain.

Slowly, researchers are gathering enough scientific evidence to clarify the impact of various brain games on cognitive health. This is an important topic because marketers of such offerings have been hyping benefits for some time while academic skeptics have been sounding cautionary alarms. Until now, both sides have been operating in the dark or, at best, in dim light.

According to a study recently published in the Journal of the American Geriatrics Society, a group of 65+ year old subjects who engaged in daily computer-based exercises from Posit Science were able to outperform another group who spent the same amount of time watching educational DVD's and being tested on the content. This is one of the first studies that showed a correlation between computer based brain exercise and improved performance in other areas of cognition. That is, playing the games seemed to have improved mental performance in exercises other than the game.

The authors of the study speculated that Lumosity, a web-based brain exercise, might also yield improvements in cognition but were much less optimistic about the benefit of the Nintendo "Brain Age" series of games.

For me, it is encouraging that sound research has begun to identify the specific types of cognitive exercises that support genreal brain health. I look forward to more answers in this area.

According to the amyloid hypothesis, a primary culprit driving cognitive decline in Alzheimer's patients is the presence of amyloid beta protein oligomers that aggregate into toxic plaques in the brain. A study out of UCLA and published in the Proceedings of the National Academy of Sciences has shed new light on the relative toxicity among oligomers of different sizes and structures.

This new understanding showed that size matters with larger oligomers being more toxic than smaller ones. Importantly, the structure of the oligomers was more important than size in determining toxicity. In fact, toxicity increased exponentially as the structure of the underlying oligomer became more complex.

This new understanding could be greatly beneficial to researchers seeking novel treatment strategies for Alzheimer's disease. By targeting amyloid in its most toxic forms, researchers may be closer to developing more effective treatments.

One of the barriers to faster drug development is the time it takes to recruit well-characterized research subjects into a clinical trial.

Consider this example: if a trial needs 2000 people over the age of 65 who have been diagnosed with mild to moderate Alzheimer's then it is drawing from a total pool of no more than 2-3 million people in the USA. If the protocol excludes research subjects who are currently taking a cholinesterase inhibitor (the most common class of prescription drugs for AD), then the pool is cut approximately in half. Additional common exclusions for other diseases and/or treatments reduce the target population further. Seeking 2000 people from a national pool of a million or so, while in competition with more than a dozen other trials who wish to recruit the same people is a daunting task. It can take a long time.

Sadly, there are people who wish to enroll in trials but are unaware of them. Despite the efforts of the drug development groups, it is impossible to blanket the country with perfect information in real time. There is always a knowledge gap between the needs of the clinical trialists and the information held by the public.

Pfizer is taking what seems to be an intelligent step in the direction of solving this problem. They are preparing to launch a website where potential research subjects can register and share personal, medical information about themselves in a protected environment. From this database, clinical trialsts will be able to more efficiently identify and contact those subjects who would qualify for a particular trial. Hopefully, this electronic marketplace will reduce the lag between the initiation of a trial and the time when it is fully enrolled.

I expect that many will not trust a pharmaceutical company to hold their medical information without trying to exploit it for some commercial benefit. However, I suspect many others, who are keenly interested in gaining access to experimental drugs, will be willing. Pfizer and the rest of their brethren have tremendous incentives (including legal incentives) to use this information only for its stated purpose and I believe they will.

Overall, I think this is a great idea that could meaningfully accelerate drug development and produce the better AD treatments that we so desperately need.

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As scientists generate new hypotheses about Alzheimer's pathology and assimilate new findings into the iterative storm of research in this area, new light reaches the topic on a daily basis. As reported recently in The Journal of Neuroscience, a study out of the Salk Institute may have uncovered an important piece of information about nicotine receptors and their role in the problem.

Alpha-7 is a nicotine receptor known to play a key role in certain cognitive processes. Based on this knowledge, scientists have sought potential treatments that activate this receptor theorizing that it might improve cognition in Alzheimer's patients. Findings have suggested something quite different.

In this study, researchers used genetically engineered mice with two particular mutations. First, they were prone to over-production of amyloid precursor protein (APP) which plays a key role in the formation of amyloid plaques in Alzheimer's patients. Second, they lacked the gene for the alpha-7 receptor. The expectation was that these mice, lacking alpha-7 receptors, would under-perform other mice with only the first mutation (prone to producing APP). Such a finding would help to demonstrate the helpful role of the nicotine receptors.

Surprisingly, these cross-engineered mice performed as well on memory tests as normal mice and outperformed mice that over produced APP but had intact alpha-7 receptors. The preliminary conclusion is that it must be the combination of APP and the alpha-7 receptors that triggers the cognitive decline in Alzheimer's patients. This is somewhat different than expected but serves as a perfect example of the scientific process of discovery in action.

For future direction, scientists might explore agents that block APP from interacting with the alpha-7 receptors as opposed to the past approach of merely stimulating the receptors.

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Last week, the LA Times published a good overview on some recent studies about reducing risks for Alzheimer's disease.

Among the risks described were high blood pressure, diabetes, obesity, smoking and high-fat diets. Among those preventative approaches highlighted by recent press were the so-called Mediterranean diet and exercising regularly. Other lifestyle factors, such as doing the daily crossword puzzle and/or maintaining an active social life have been associated with lowered Alzheimer's risk and were briefly discussed.

CausalityA key feature that I appreciated in this overview, one that I notice is often neglected in the popular press, was the careful treatment of "causal relationships". Although many "risks" (i.e. high cholesterol, smoking, etc.) are associated with higher incidence of Alzheimer's disease, they may not represent a direct causal relationship.

The correlation between certain conditions and a higher or lower incidence of disease gives scientists the opportunity to generate and test hypotheses but most of the studies we read about today are not as definitive as the headlines often indicate. This particular article is exemplar in its description of causality and the tone of its conclusions.

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There has been ongoing debate between the advocates for knowing one's genetic risk for Alzheimer's disease and those who think the information is useless if not harmful. The respective arguments break out as follows:

In favor of knowing genetic riskThe knowledge will relieve the needlessly worried (when the genetic risks are low) and may encourages a more proactive approach toward managing other risk factors (when the genetic risks are high).

Against knowing genetic riskThe knowledge may lead to undue anxiety and depression among those with high genetic risks, especially since there is no cure for Alzheimer's disease.

I think the argument against "knowing" is weak for a couple of reasons. First, it is purely speculative and second, it undersells the effectiveness of current treatments in some patients, especially when intervention occurs at an early stage of the disease. According to new research out of Boston University and published in the New England Journal of Medicine, the argument against knowing is indeed weak.

In a study of 162 asymptomatic adults with a parent who had Alzheimer's disease, researchers randomly divided the research subjects into two groups, one of which would learn their genetic information and one which would not. At follow up periods of 6 weeks, 6 months, and 1 year, participants were assessed for symptoms of anxiety, depression, and test-related distress and the results were compared across the two groups. The results showed no significant increase in emotional distress among those who learned of a high genetic risk while showing a reduction in emotional distress among those who learned that their risks were low.

To be clear, I don't think anyone should have such information thrust upon them if they don't wish to know. But among the increasingly well-educated consumers of health care, there is an appetite for information and I support everyone's right to know about their own risks.

The results of this study bode well for the campaign to identify those at risk for a memory disorder and to intervene in a timely manner. Doing so may be an important step toward optimizing health and preserving quality of life.

This is a topic about which there is much debate in the press and often, the writers are poorly informed. If you found this useful, please share it by adding the link to your Facebook page, by Digging the article, or by distributing via email/Twitter as you prefer. The "share" button enabling these services and others is below.

We all know this intuitively but it bears repeating. Another study, this one out of Columbia University and published in the Journal of the American Medical Association, has demonstrated the benefits of diet and exercise in mitigating the risks for Alzheimer's disease.

This was a massive study on 1,880 people spanning 14 years and the results were clear. Those subjects who most closely adhered to the recommended Mediterranean diet reduced their risk by 40% and those with the most regular exercise regimens reduced their risk by 33%.

Everyone is busy and life is hectic but there is really no legitimate excuse for not taking care of your brain and your heart through a sensible diet and some form of regular physical exercise. Please share this message at every opportunity.

A better understanding and more awareness of Alzheimer's related issues can impact personal health decisions and generate significant impact across a population of aging individuals. Please use the share button below to spread this educational message as widely as possible.

Although physicians are fairly precise in their discourse amongst themselves, they sometimes use the term "stroke" with the lay-public to describe a wide range of occurrences in the brain. A new study published in Neurology suggests that we might all benefit from the practice of more carefully characterizing one form of stroke from another.

In a study at Columbia University, researchers looked at brain scans of 679 subjects aged 65 and older and compared those with white matter hyperintensities to those with areas of dead brain tissue. The first group had suffered what is sometimes called "mini-stroke" and were more than twice as likely to have mild cognitive impairment with memory loss compared to the latter group of stroke victims that was more likely to have mild cognitive impairment without memory loss.

The key finding was that the different events (mini-stroke vs. stroke) led to different types of cognitive problems. While mini-strokes and strokes have traditionally been considered as originating from the same source, this study suggests they might be quite different.

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This fact has great "face validity" and makes sense to most of us. More evidence of the value of mental activity was published last week in Neurology.

According to a five-year study on 488 persons aged 75-85, participating in at least 11 mentally rigorous exercises per week had a decelerating effect on memory loss among those who were demented. To clarify, the study found that, if one becomes demented due to some medical condition and, if one stays very mentally active, the expected decline in memory will be delayed compared to those demented persons who are not as mentally active.

One key point is that the study participants who were shown to delay memory loss participated in a high number (eleven) of diverse mental exercises per week. This does not suggest that the daily crossword or computer game will produce the same effect. While all mental activity is probably useful in some capacity, it is important to note that the effects in this study were produced with a fairly rigorous agenda of mental activity.

The bottom line is that exercising the brain adequately may feel more like work than like play but the benefits are likely worth the effort.

In a study published last week in Neuron, researchers at the University of Pennsylvania found a high correlation between amyloid plaque formation and decreasing brain function. This is consistent with the amyloid hypothesis that such plaques play a central role in Alzheiemr's disease.

One weakness of this hypothesis has been the discovery of older people with heavy plaque loads in their brains and no memory loss. Some have suggested that this is evidence that another culprit, distinct from or in addition to amyloid, must be causing the loss of cognitive function.

In this present study, researchers noted a correlation between the accumulation of plaques and the activity in a key neural circuit associated with epidosic memory formation. With this research, a nuanced view is that the amyloid plaques interfere with the process of memory formation but the brain compensates and continues to function adequately for some time as the plaque load increases.

In this way, the amyloid hypothesis may still explain impaired memory but through a more complex process that takes longer to play out. As such, it would be possible for an individual to maintain a high plaque load and to preserve short-term memory for some period of time.

One of the most respected researchers in the Alzheimer's field, Mark Sager at the University of Wisconsin in Madison, has published his group's latest findings in Alzheimer's and Dementia. They concluded that the costs of not screening for Alzheimer's and not providing caregiver support costs the nation billions of dollars in avoidable public health care expenditures.

This is not surprising given the well documented correlation between progression of AD symptoms and rising costs of care. The importance of this publication lies in the fact that it is another solid piece of research arguing for a more proactive approach to battling AD.

Buried in this study is another important finding that debunks the argument against screening for memory loss. While some have speculated that seeking signs of memory loss among the presumed healthy stirs up unnecessary angst about the specter of Alzheimer's disease. Angst they characterize as "not constructive" given that no cure for AD is at hand.

Contrarily, this study showed that many people diagnosed with AD were relieved. This finding is consistent with several smaller studies that have shown the same result. The take away is this: if our ability to manage the disease is improved through early diagnosis and the people who undergo memory assessment are happier to have done so, then the benefits of a proactive, early-intervention program are amplified.

If we can continue to tear down the argument against earlier intervention while demonstrating the health and economic benefits of doing so, we will be much more effective in managing this disease, even before a cure is found.

A better understanding and more awareness of Alzheimer's related issues can impact personal health decisions and generate significant impact across a population of aging individuals. Please use the share button below to spread this educational message as widely as possible.

With today's release of a study from Kaiser Permanente, published in the journal Dementia & Geriatrics Cognitive Disorders, we have strong evidence that even borderline high cholesterol in mid-life (aged 40-45) significantly raises the risk of dementia in later life (aged 65+).

For high cholesterol, defined as 240 or higher milligrams per deciliter of blood, risk for dementia was increased by 66%. More alarming was the finding that even moderately high cholesterol (200+ milligrams per deciliter) increased risk by 52%.

The Kaiser study looked at 9,844 men and women who were 40 to 45 years old between 1964 and 1973 when their cholesterol levels were first collected. Of the total participants, 469 were diagnosed with Alzheimer's disease between 1994 and 2007 when the members were between 61 and 88 years old, and 127 developed vascular dementia.

The good news is that cholesterol levels can often be modified through diet, exercise and lifestyle changes in addition to cholesterol lowering drugs. This news should serve as additional evidence about the importance of maintaining good cardiovascular health as a means of reducing risk for dementia.

Each fall, the National Alzheimer's Association helps to coordinate hundreds of local Memory Walks in the nation's communities. These walks raise funds for ongoing research and support programs and do a great deal to raise awareness of the growing prevalence of Alzheimer's disease.

I encourage each and every reader of this blog to consider participating in a memory walk this year. Aside from the obvious benefits of participating in such a good cause, they are extremely inspiring events with many participants walking in the memory of a loved one. The atmosphere is always charged with emotion and touching tributes.

Also, because one of the biggest barriers to better care in this field is late detection of the problem, we really need to start lifting the stigma that prevents many people from seeking care when their symptoms are very subtle. These memory walks are fantastic vehicles for destroying that stigma. Nearly every person in the crowd will have cared for a loved one with the disease or lost a loved one to the disease. There are also a fair number of Alzheimer's patients who participate and advocate for greater visibility.

Overall, I am a strong supporter of the memory walk events and feel that they bring more than just important funds to this problem. They bring visibility and education to a growing number of citizens each year and I hope each of you will consider participating and contributing to one of these programs this year.